Why don't mitochondria have junk DNA?
John Harshman
do mitochondria have to replicate that often compared to the nucleus of
the same cell? That would depend on the lifetime of a mitochondrion and
its standing population in the cell. I'll have to look that up.
If not that, then what?
There are mitochondria with junk. In fact the control region has been
duplicated several times in different groups of birds, and one of the
copies is clearly non-functional. So it does happen. But why so rarely?
r norman
To demonstrate solidarity with their old comrades-in-arms?
Is there something about the structure of a prokaryotic genome that
tends to enforce the lack of junk? about the factors that can allow
junk to creep in during replication? Do mitochondria get phage
infections?
On another tack, why don't we hear about much about the chloroplast
genome? Is it just my chauvinistic animal kingdomism? Or that there
are too many cases of paternal inheritance -- all gymnosperms, for
example?
Steve Schaffner
I hear about the apicoplast genome, but that probably just reflects
the people I've been hanging around lately.
--
Steve Schaffner s...@broad.mit.edu
Immediate assurance is an excellent sign of probable lack of
insight into the topic. Josiah Royce
John Harshman
> On Wed, 04 Jan 2006 00:16:20 GMT, John Harshman
> <jharshman....@pacbell.net> wrote:
>
>
>>Selection for fast replication? That's the usual idea for bacteria, but
>>do mitochondria have to replicate that often compared to the nucleus of
>>the same cell? That would depend on the lifetime of a mitochondrion and
>>its standing population in the cell. I'll have to look that up.
>>
>>If not that, then what?
>>
>>There are mitochondria with junk. In fact the control region has been
>>duplicated several times in different groups of birds, and one of the
>>copies is clearly non-functional. So it does happen. But why so rarely?
>
>
> To demonstrate solidarity with their old comrades-in-arms?
>
> Is there something about the structure of a prokaryotic genome that
> tends to enforce the lack of junk? about the factors that can allow
> junk to creep in during replication?
Nothing that I can think of. That's why I asked.
> Do mitochondria get phage
> infections?
I don't know. There would seem to be reasons against it. Once the phage
lyses all the mitochondria in a single cell, where does it go from
there? It would take a complicated phage to get through all the
membranes going in, and half of them going out.
> On another tack, why don't we hear about much about the chloroplast
> genome? Is it just my chauvinistic animal kingdomism?
Yes. If you hung out with botanists you would hear plenty about
chloroplast genomes.
[snip]
John Wilkins
You hang with parasites?
--
John S. Wilkins, Postdoctoral Research Fellow, Biohumanities Project
University of Queensland - Blog: evolvethought.blogspot.com
Servum tui ero, ipse vespera
r norman
<jharshman....@pacbell.net> wrote:
>r norman wrote:
>
>> On another tack, why don't we hear about much about the chloroplast
>> genome? Is it just my chauvinistic animal kingdomism?
>
>Yes. If you hung out with botanists you would hear plenty about
>chloroplast genomes.
>
Yuck! Why in the world would I ever want to hang out with them?
Dale
news:otEuf.6229$UF3....@newssvr25.news.prodigy.net...
Is there even room for junk in mitochondrial DNA? Haven't mitochondria given
up some DNA in favor of a symbiotic relationship?
And consider if mutated junk DNA has anything to do with phenotype. If a
mitochondrion had some junk DNA, and then there were a mutation that
activated the junk and made it non-junk, then it might become more like an
invader than a symbiont. So anything that had mitochondria with a lot of
junk would have a tendency to die a horrible death, and then of course that
would be the end of the line for that mitochondrial "species".
Okay, I'm just pulling stuff out of my ass here, I've been reading a
textbook on molecular cell biology, but maybe there's something there that
can help.
Steve Schaffner
According to my father-in-law, yes. Parasites include academics,
clergymen and insurance salesmen. (Fortunately, he's polite enough
not to press that point of view on those of his children who are
academics.) On the other hand, some of us may get a pass, since we're
supposedly fighting disease.
An alternative explanation is that I spend too much time hanging
around the spleen.
Dale
news:ydlsls4...@phosphorus.broad.mit.edu...
[...]
> An alternative explanation is that I spend too much time hanging
> around the spleen.
The spleen! Back when they took mine out, they said it was no biggie to not
have a spleen. Is that still considered true? I haven't had a spleen for 31
years, and it seems okay, but how do I know what I'm missing?
rev.goetz
Junk DNA is an extavagant byproduct of evolutionary processes because
the rate of neutral mutational insertions from various types of
repeated sequences appears to be significantly more frequent than the
fixation rate of all mutational deletions. And I recall that only
diploid cells have the mechanisms that generate various types of
repeated sequences. (I do not have the time to look up the reasons for
this.)
Concerning some junk DNA in mitochondria, this could have occurred by
DNA transfer from the nuclear genome to the mitochondrial genome. I am
not sure if I have heard of cases of DNA transfer from the nuclear
genome to the mitochondrial genome, but I know that I heard of several
examples of gene transfer from the mitochondrial genome to the the
nuclear genome. So I would not be surprised to see if the reverse ever
happened.
John Wilkins
merozoites (I think - it's been a while since I read this stuff) and so are in
greater risk of a stroke. Of course this is only likely if you travel to
regions where that parasite is endemic.
Steve Schaffner
> Dale wrote:
> > "Steve Schaffner" <s...@phosphorus.broad.mit.edu> wrote in message
> > news:ydlsls4...@phosphorus.broad.mit.edu...
> > [...]
> >
> >>An alternative explanation is that I spend too much time hanging
> >>around the spleen.
> >
> >
> > The spleen! Back when they took mine out, they said it was no biggie to not
> > have a spleen. Is that still considered true? I haven't had a spleen for 31
> > years, and it seems okay, but how do I know what I'm missing?
> >
> If you get Plasmodium falciparum, you will have trouble eliminating the
> merozoites (I think - it's been a while since I read this stuff) and so are in
> greater risk of a stroke. Of course this is only likely if you travel to
> regions where that parasite is endemic.
Splenectomy increases the risk of bacterial infection (of several
kinds), as well as of malaria. Hence patients usually receive
vaccinations (for pneumonia and menningitis) and sometimes
prophylactic antibiotics. Mostly adults do just fine without a
spleen. Or so I read -- I am not a physician.
Larry Moran
John Harshman <jharshman....@pacbell.net> wrote:
> r norman wrote:
[snip]
>> Is there something about the structure of a prokaryotic genome that
>> tends to enforce the lack of junk? about the factors that can allow
>> junk to creep in during replication?
>
> Nothing that I can think of. That's why I asked.
Prokarotic genomes have a single origin of DNA replication. The entire
genome (usually circular) has to be replicated by complexes that start
at a unique site and move off in both directions until they meet at a
termination region opposite the orign.
bioinfo.med.utoronto.ca/~lamoran/bidirectional_DNA_replication.jpg
As the genome expands, replication takes longer and longer because the
replication forks have to travel further before they meet and terminate.
Not only does this mean that division will be slowed but it also increases
the risk that the replication complex will fall off before it finishes.
(The complex is highly processive, which means that it usually sticks to
the DNA until the job is finished, but there's a finite chance that it
won't.)
For these reasons, there is selection against expanding prokaryotic genomes
by accumulating junk DNA. In the case of bacteria with large genomes, the
problem is solved by having more than one chromosome but the mechanisms
for segregating chromsomes are sloppy so you can't have too many.
Eukaryotes have multiple origins of replication on every chromosome and
each replication complex only has to travel about as far as a typical
bacterial complex. It's easy to duplicate replication origins so expansion
of the genome doesn't have the same severe consequences as it does for
bacteria. Furthermore, you can have dozens of chromosomes because
mitosis and meiosis are very efficient ways of segregating chromosomes.
Eukaryotic genomes evolved ways of handling larger genomes because they
need more genes. The solutions were so good that the presence of large
amounts of junk DNA had little effect on the viability of multicellular
species.
Larry Moran
r norman
wrote:
Just what do you vent when you are angry?
chris.li...@gmail.com
What do you think is the root of your hostility toward botanists?
Chris
Friar Broccoli
> Prokarotic genomes have a single origin of DNA replication. The entire
> genome (usually circular) has to be replicated by complexes that start
> at a unique site and move off in both directions until they meet at a
> termination region opposite the orign.
Please excuse this interruption from an idiot, but are you saying:
1) That mitochondria was originally a prokaryote (not a eukaryote
like the rest of me)?
2) That mitochondria still replicate in exactly the same way
prokaryotes (bacteria etc) do?
Supplementary:
As I recall one of the 3 letter DNA words in the mitochondria
code for a different amino acid than elsewhere in the cell.
Is that transcription the same as that commonly found in
prokaryotes?
>
> bioinfo.med.utoronto.ca/~lamoran/bidirectional_DNA_replication.jpg
>
> As the genome expands, replication takes longer and longer because the
> replication forks have to travel further before they meet and terminate.
> Not only does this mean that division will be slowed but it also increases
> the risk that the replication complex will fall off before it finishes.
> (The complex is highly processive, which means that it usually sticks to
> the DNA until the job is finished, but there's a finite chance that it
> won't.)
>
> For these reasons, there is selection against expanding prokaryotic genomes
> by accumulating junk DNA. In the case of bacteria with large genomes, the
> problem is solved by having more than one chromosome but the mechanisms
> for segregating chromsomes are sloppy so you can't have too many.
>
> Eukaryotes have multiple origins of replication on every chromosome and
> each replication complex only has to travel about as far as a typical
> bacterial complex. It's easy to duplicate replication origins so expansion
> of the genome doesn't have the same severe consequences as it does for
> bacteria. Furthermore, you can have dozens of chromosomes because
> mitosis and meiosis are very efficient ways of segregating chromosomes.
>
> Eukaryotic genomes evolved ways of handling larger genomes because they
> need more genes. The solutions were so good that the presence of large
> amounts of junk DNA had little effect on the viability of multicellular
> species.
>
>
>
> Larry Moran
Cordially;
Friar Broccoli
Robert Keith Elias, Quebec, Canada Email: EliasRK (of) gmail * com
Best programmer's & all purpose text editor: http://www.semware.com
--------- I consider ALL arguments in support of my views ---------
John Harshman
That's a nice explanation for bacteria, but what about mitochondria?
They have teeny little genomes, much smaller than any bacterium
(especially in metazoans). So they can't possibly be up against a
replicative wall. Yet they have approximately no junk.
John Harshman
> "John Harshman" <jharshman....@pacbell.net> wrote in message
> news:otEuf.6229$UF3....@newssvr25.news.prodigy.net...
>
>>Selection for fast replication? That's the usual idea for bacteria, but
>>do mitochondria have to replicate that often compared to the nucleus of
>>the same cell? That would depend on the lifetime of a mitochondrion and
>>its standing population in the cell. I'll have to look that up.
>>
>>If not that, then what?
>>
>>There are mitochondria with junk. In fact the control region has been
>>duplicated several times in different groups of birds, and one of the
>>copies is clearly non-functional. So it does happen. But why so rarely?
>
>
> Is there even room for junk in mitochondrial DNA? Haven't mitochondria given
> up some DNA in favor of a symbiotic relationship?
What do you mean by "room"?
> And consider if mutated junk DNA has anything to do with phenotype.
It doesn't. That's why it's junk.
> If a
> mitochondrion had some junk DNA, and then there were a mutation that
> activated the junk and made it non-junk, then it might become more like an
> invader than a symbiont. So anything that had mitochondria with a lot of
> junk would have a tendency to die a horrible death, and then of course that
> would be the end of the line for that mitochondrial "species".
Highly doubtful. And of course that explanation applies (if it applies
at all) much more to your nucleus than your mitochondria. Yet your
nucleus tolerates a large majority of junk.
John Harshman
> John Harshman wrote:
>
>>Selection for fast replication? That's the usual idea for bacteria, but
>>do mitochondria have to replicate that often compared to the nucleus of
>>the same cell? That would depend on the lifetime of a mitochondrion and
>>its standing population in the cell. I'll have to look that up.
>>
>>If not that, then what?
>>
>>There are mitochondria with junk. In fact the control region has been
>>duplicated several times in different groups of birds, and one of the
>>copies is clearly non-functional. So it does happen. But why so rarely?
>
>
> Junk DNA is an extavagant byproduct of evolutionary processes because
> the rate of neutral mutational insertions from various types of
> repeated sequences appears to be significantly more frequent than the
> fixation rate of all mutational deletions. And I recall that only
> diploid cells have the mechanisms that generate various types of
> repeated sequences. (I do not have the time to look up the reasons for
> this.)
You would seem to be talking about unequal crossing over. That's only
one of a host of processes that generate new sequences.
> Concerning some junk DNA in mitochondria, this could have occurred by
> DNA transfer from the nuclear genome to the mitochondrial genome. I am
> not sure if I have heard of cases of DNA transfer from the nuclear
> genome to the mitochondrial genome, but I know that I heard of several
> examples of gene transfer from the mitochondrial genome to the the
> nuclear genome. So I would not be surprised to see if the reverse ever
> happened.
I don't know of any such case. Like I said, the only mt junk I know of
involves a duplication of a mitochondrial region.
John Harshman
> Larry Moran wrote:
>
>
>>Prokarotic genomes have a single origin of DNA replication. The entire
>>genome (usually circular) has to be replicated by complexes that start
>>at a unique site and move off in both directions until they meet at a
>>termination region opposite the orign.
>
>
> Please excuse this interruption from an idiot, but are you saying:
>
> 1) That mitochondria was originally a prokaryote (not a eukaryote
> like the rest of me)?
Yes, he is. This is almost universally accepted, thanks to the efforts
of Lynn Margulis.
> 2) That mitochondria still replicate in exactly the same way
> prokaryotes (bacteria etc) do?
Yes, he is. This is true too. Circular chromosome, single origin of
replication, prokaryote-type replication enzymes (though currently coded
for by nuclear genes, at least in metazoans).
> Supplementary:
>
> As I recall one of the 3 letter DNA words in the mitochondria
> code for a different amino acid than elsewhere in the cell.
> Is that transcription the same as that commonly found in
> prokaryotes?
No. Most prokaryotes have the same code as most eukaryote nuclei. There
are a number of slight variants found in various parts of the tree of
life. Mitochondria are no exception, and in fact have more frequent
variants. Your mitochondrial code is in fact different in several
respects from your nuclear code. But this has nothing to do with the
mitochondrion's relationship to prokaryotes.
[snip]
r norman
<chris.li...@gmail.com> wrote:
>r norman wrote:
>> On Wed, 04 Jan 2006 02:22:19 GMT, John Harshman
>> <jharshman....@pacbell.net> wrote:
>>
>> >r norman wrote:
>> >
>> >> On another tack, why don't we hear about much about the chloroplast
>> >> genome? Is it just my chauvinistic animal kingdomism?
>> >
>> >Yes. If you hung out with botanists you would hear plenty about
>> >chloroplast genomes.
>> >
>>
>> Yuck! Why in the world would I ever want to hang out with them?
>
>What do you think is the root of your hostility toward botanists?
>
I won't beat around the bush. It stems from an old but fruitless
relation that I still pine for. What a sap I was!
chris.li...@gmail.com
Ah. You probably lost this relation to a rival. When you mentioned
'hanging around' I immediately conjured up images of a grand
competition- an epic fight, as it were. Or, kidding aside, you should
start exercising- get to the gym, no spur makes you feel better than a
good workout.
Chris
rev.goetz
John Harshman wrote:
> rev.goetz wrote:
>
> > John Harshman wrote:
> >
> >>Selection for fast replication? That's the usual idea for bacteria, but
> >>do mitochondria have to replicate that often compared to the nucleus of
> >>the same cell? That would depend on the lifetime of a mitochondrion and
> >>its standing population in the cell. I'll have to look that up.
> >>
> >>If not that, then what?
> >>
> >>There are mitochondria with junk. In fact the control region has been
> >>duplicated several times in different groups of birds, and one of the
> >>copies is clearly non-functional. So it does happen. But why so rarely?
> >
> >
> > Junk DNA is an extavagant byproduct of evolutionary processes because
> > the rate of neutral mutational insertions from various types of
> > repeated sequences appears to be significantly more frequent than the
> > fixation rate of all mutational deletions. And I recall that only
> > diploid cells have the mechanisms that generate various types of
> > repeated sequences. (I do not have the time to look up the reasons for
> > this.)
>
> You would seem to be talking about unequal crossing over. That's only
> one of a host of processes that generate new sequences.
Unequal crossing over is only one of a few mechanisms that help to
generate non-coding DNA in eukaryotes.
>
> > Concerning some junk DNA in mitochondria, this could have occurred by
> > DNA transfer from the nuclear genome to the mitochondrial genome. I am
> > not sure if I have heard of cases of DNA transfer from the nuclear
> > genome to the mitochondrial genome, but I know that I heard of several
> > examples of gene transfer from the mitochondrial genome to the the
> > nuclear genome. So I would not be surprised to see if the reverse ever
> > happened.
>
> I don't know of any such case. Like I said, the only mt junk I know of
> involves a duplication of a mitochondrial region.
I missed that you said it was a duplication of a mitochondrial region,
so scratch what I said about DNA transfer from the nuclear genome to
the mitochondrial genome.
In general, mutational insertions/duplications are more likely to occur
in eukaryotes compared to prokaryotes. And as someone said earlier in
this topic, many eukaryotes are not harmed by an accumulation of DNA in
the genome. So many insertions/duplications are neutral in terms of
fitness in many eukaryotes, but in many prokaryotes a large increase in
genome size causes a decrease in fitness. So natural selection prevents
a large increase of "useless DNA"in many prokaryotes.
John Harshman
> John Harshman wrote:
>
>>rev.goetz wrote:
>>
>>
>>>John Harshman wrote:
>>>
>>>
>>>>Selection for fast replication? That's the usual idea for bacteria, but
>>>>do mitochondria have to replicate that often compared to the nucleus of
>>>>the same cell? That would depend on the lifetime of a mitochondrion and
>>>>its standing population in the cell. I'll have to look that up.
>>>>
>>>>If not that, then what?
>>>>
>>>>There are mitochondria with junk. In fact the control region has been
>>>>duplicated several times in different groups of birds, and one of the
>>>>copies is clearly non-functional. So it does happen. But why so rarely?
>>>
>>>
>>>Junk DNA is an extavagant byproduct of evolutionary processes because
>>>the rate of neutral mutational insertions from various types of
>>>repeated sequences appears to be significantly more frequent than the
>>>fixation rate of all mutational deletions. And I recall that only
>>>diploid cells have the mechanisms that generate various types of
>>>repeated sequences. (I do not have the time to look up the reasons for
>>>this.)
>>
>>You would seem to be talking about unequal crossing over. That's only
>>one of a host of processes that generate new sequences.
>
> Unequal crossing over is only one of a few mechanisms that help to
> generate non-coding DNA in eukaryotes.
It's the only one I know of that relies on diploidy.
>>>Concerning some junk DNA in mitochondria, this could have occurred by
>>>DNA transfer from the nuclear genome to the mitochondrial genome. I am
>>>not sure if I have heard of cases of DNA transfer from the nuclear
>>>genome to the mitochondrial genome, but I know that I heard of several
>>>examples of gene transfer from the mitochondrial genome to the the
>>>nuclear genome. So I would not be surprised to see if the reverse ever
>>>happened.
>>
>>I don't know of any such case. Like I said, the only mt junk I know of
>>involves a duplication of a mitochondrial region.
>
> I missed that you said it was a duplication of a mitochondrial region,
> so scratch what I said about DNA transfer from the nuclear genome to
> the mitochondrial genome.
>
> In general, mutational insertions/duplications are more likely to occur
> in eukaryotes compared to prokaryotes. And as someone said earlier in
> this topic, many eukaryotes are not harmed by an accumulation of DNA in
> the genome. So many insertions/duplications are neutral in terms of
> fitness in many eukaryotes, but in many prokaryotes a large increase in
> genome size causes a decrease in fitness. So natural selection prevents
> a large increase of "useless DNA"in many prokaryotes.
As I theorized at the outset. But can this possibly apply to
mitochondria? Larry's mechanism obviously can't, since mt genomes are
tiny by comparison with bacterial genomes. The other suggested
mechanism, selection for speedy replication, also would seem not to be
that strong in mitochondria, though that would depend on their
population genetics. I really have to dig this up and read it again:
Birky, C. W., Jr. 1991. Evolution and population genetics of organelle
genes: Mechanisms and models. Pages 112-134 In R. K. Selander, A. G.
Clark and T. S. Whittam (eds), Evolution at the Molecular Level. Sinauer
Assoc., Sunderland, MA.
Ernest Major
<NotMyRealEmail@_comcast.net> writes
>
>On another tack, why don't we hear about much about the chloroplast
>genome? Is it just my chauvinistic animal kingdomism? Or that there
>are too many cases of paternal inheritance -- all gymnosperms, for
>example?
>
work with cpDNA than with mtDNA. About a score of complete embryophyte
chloroplast genomes have been sequenced.
BTW, chloroplast genomes have introns and, IIRC, other junk.
--
alias Ernest Major
--
No virus found in this outgoing message.
Checked by AVG Free Edition.
Version: 7.1.371 / Virus Database: 267.14.10/218 - Release Date: 02/01/2006
Ken Shackleton
Maybe his ass?
rev.goetz
Even though mitochondria has a small genome size compared to
prokaryotes, natural selection favoring a compact genome could still be
the primary force that keeps it compact. For example, we know by theory
that mitochondria ancestors once had a complete prokaryote genome when
they were prokaryotes. And I conjecture that natural selection favoring
compactness helped to reduce the mitochondrial genomes to their current
sizes. And I see no reason why anything else but natural selection
favoring compactness would be needed to keep the mitochondrial genomes
near their current sizes.
On the otherhand, I know nothing about "selection for speedy
replication" so I cannot comment about that.
John Harshman
It's a form of selection for compactness. Unless you can suggest a
reason why compactness would be selected, all you are saying is that
selection produces whatever you happen to see, i.e. you are falling
victim to the panglossian paradigm. I'm saying that I have trouble
figuring out a reason why compactness (one or two orders of magnitude
more compactness than in a bacterium) should be selected here.
No selection is required in order for mt genes to be transferred to the
nucleus, by the way. Just 1) transfer of a functional copy of a mt gene
into the nucleus followed by 2) decay of the mt copy, no longer
maintained by selection.
Larry Moran
> Larry Moran wrote:
>
>> Prokarotic genomes have a single origin of DNA replication. The entire
>> genome (usually circular) has to be replicated by complexes that start
>> at a unique site and move off in both directions until they meet at a
>> termination region opposite the orign.
>
> Please excuse this interruption from an idiot, but are you saying:
>
> 1) That mitochondria was originally a prokaryote (not a eukaryote
> like the rest of me)?
Yes.
> 2) That mitochondria still replicate in exactly the same way
> prokaryotes (bacteria etc) do?
Not "exactly" but close enough.
> Supplementary:
>
> As I recall one of the 3 letter DNA words in the mitochondria
> code for a different amino acid than elsewhere in the cell.
> Is that transcription the same as that commonly found in
> prokaryotes?
In some species the mitochondrial genetic code differs slightly from the
standard genetic code. The same standard genetic code is used in prokaryotes
and eukaryotes so this is not due to the prokaryotic origin of mitochondria.
Protein coding genes are *transcribed* to produce mRNA and the mRNA is
*translated* to produce a protein. During *transcription* the DNA sequence is
merely copied into RNA (transcription = copying). The actual *translation* of
the nucleotide sequence according to the genetic code occurs during protein
synthesis (translation = converting nucleotide sequence to polypeptide
sequence).
Larry Moran
r norman
Mitochondria also have their own variety of ribosomes, different from
both the eukaryotic and the prokaryotic variety.
Larry Moran
John Harshman <jharshman....@pacbell.net> wrote:
> Larry Moran wrote:
[snip]
> That's a nice explanation for bacteria, but what about mitochondria?
> They have teeny little genomes, much smaller than any bacterium
> (especially in metazoans). So they can't possibly be up against a
> replicative wall. Yet they have approximately no junk.
The same basic principles apply to mitochondrial genomes but there are
some complications. The actual mechanism of DNA replication in mitochondria
seems to be a degenerative version of bacterial DNA replication. In most
cases there's a single-stranded intermediate produced during the
replication of mitochondrial DNA. This single-stranded intermediate is
easily degraded by endogenous nucleases.
The addition of extra DNA to the mitochondrial genome will, in many cases,
lengthen the single-stranded region and increase the time that it will
be single-stranded. (Mitochondrial DNA replication complexes don't work
as efficiently as bacterial ones.) Thus, there's probably strong negative
selection against expanding the mitochondrial genome.
Larry (who hates adaptationist explanations) Moran
John Wilkins
John Wilkins
they also share the junk of the nuclear genome...
rev.goetz
Yes, no natural selection is required. Neutral theory helps to explain
this. On the other hand, the hierarchal transfer of ribosomal protein
small unit (_rps_) genes from mitochondrial genomes to nuclear genomes
most likely resulted from natural selection because the hierarchy
relates to the importance on the functional importance of respective
the _rps_ genes.
John Harshman
Most of their functions (if by that you mean their proteins) are nuclear
coded. Would you care to develop the concept of junk-sharing in greater
detail.
John Harshman
Words missing or added here? It doesn't parse. Not sure what you mean by
"hierarchal transfer" either. At any rate, plase explain why rps
transfer to the nucleus is any less potentially the result of neutral
processes than, say, cytochrome c transfer.
John Wilkins
it might be because the functions of "junk" DNA, such as producing miRNAs to
regulate expression of "non-junk" DNA, has been shifted to the nuclear genome.
John Harshman
By "junk" I mean DNA whose sequence is not conserved over time, and
which we therefore can be fairly confident has no function. Some of it
may have a function that doesn't depend on sequence, i.e. just adding
bulk or spacing, and we could argue about whether that's really junk.
But I don't think it would change the category much either. It's very,
very unlikely that non-conserved DNA produces anything functional -- if
it did, it would be conserved, as miRNAs are. At any rate, prokaryotes
don't have such RNAs anyway, so there would have been none in the
ur-mitochondrion to be transferred to the genome.
I am unsure whether any mitochondrially-encoded mitochondrial proteins
or RNAs have any regulation of their expression either. If they do, it
was evolved after the symbiosis event. Prokaryote gene regulation is
quite simple, with operons and all. I don't think the metazoan
mitochondrion, at least, has any of that. There might be regulation of
transcription for the whole mt genome. (And I bet that the mitochondrion
is transcribed as a unit too.)
Matt Silberstein
<dmg...@nspm.airmail.net> in
<X1Juf.47051$q%.22096@newssvr12.news.prodigy.com> wrote:
>"Steve Schaffner" <s...@phosphorus.broad.mit.edu> wrote in message
>news:ydlsls4...@phosphorus.broad.mit.edu...
>[...]
>> An alternative explanation is that I spend too much time hanging
>> around the spleen.
>
>The spleen! Back when they took mine out, they said it was no biggie to not
>have a spleen. Is that still considered true? I haven't had a spleen for 31
>years, and it seems okay, but how do I know what I'm missing?
There is a researcher, whose name I don't remember, who thinks there
is a role of the spleen in diabetes. IIRC she thinks that some cells
migrate from the spleen to the pancreas. Supposedly there is a
significant correlation between spleen removal and subsequent
diabetes. And, more interestingly, supposedly she can transplant
something from the spleen and re-introduce insulin production.
--
Matt Silberstein
Do something today about the Darfur Genocide
http://www.beawitness.org
http://www.darfurgenocide.org
http://www.savedarfur.org
"Darfur: A Genocide We can Stop"
Matt Silberstein
<jharshman....@pacbell.net> in
<U2Tuf.10114$oW....@newssvr11.news.prodigy.com> wrote:
>Friar Broccoli wrote:
>
>> Larry Moran wrote:
>>
>>
>>>Prokarotic genomes have a single origin of DNA replication. The entire
>>>genome (usually circular) has to be replicated by complexes that start
>>>at a unique site and move off in both directions until they meet at a
>>>termination region opposite the orign.
>>
>>
>> Please excuse this interruption from an idiot, but are you saying:
>>
>> 1) That mitochondria was originally a prokaryote (not a eukaryote
>> like the rest of me)?
>
>Yes, he is. This is almost universally accepted, thanks to the efforts
>of Lynn Margulis.
I think that was the coolest "revolution" in biology that is almost
entirely unknown to the general public.
[snip]
rev.goetz
I do not know enough about cytochrome c to make the comparison, but I
will try to explain the hierarchy and the relationship to natural
selection. Buratovich (2005) notes an approximate hierarchy in the
transfer of rps genes from the mitochondrial genome to the nuclear
genome based on a comparison of 14 species. The approximate hierarchy
follows: rps1, rps10, rps11, rps2, rps7, rps8, rps4, rps19, rps19,
rps13, rps14, rps12, and rps3.
The genes that encode the proteins that are more vital for ribosomal
function are more likely to be transferred and preserved according to
the probabilities of natural selection. Likewise, the genes that encode
proteins that are less important to ribosomal function are less likely
to be transferred and preserved according to the probabilities of
natural selection.
Buratovich (June 2005) _Perspectives on Science and Christian Faith_.
Table 2, p.107.
John Harshman
Still not clear what "hierarchy" means here. Do you mean that there is
an ordering to the probability of transfer, with one end high and the
other end low? Or that transfer of one gene on the list is a
prerequisite for transfer of the next? Or what?
> The genes that encode the proteins that are more vital for ribosomal
> function are more likely to be transferred and preserved according to
> the probabilities of natural selection. Likewise, the genes that encode
> proteins that are less important to ribosomal function are less likely
> to be transferred and preserved according to the probabilities of
> natural selection.
Why?
bre...@aintitcoolmail.com
I have two thoughts here. 1) Are mitochondria subject to increased
selection pressure because they are competing amongst themselves within
the cell?, and 2) could there be some error-check mechanism in the
nuclear genome that reduces mitochondrial mutations or cause apoptosis
in mutant mitos?
DLTBWYD, Brent
rev.goetz
The hierarchy includes both the historical sequence of the transfer and
the probability of the transfer. The sequence, however, is not a
prerequisite, but a typical order with occasional exceptions.
>
> > The genes that encode the proteins that are more vital for ribosomal
> > function are more likely to be transferred and preserved according to
> > the probabilities of natural selection. Likewise, the genes that encode
> > proteins that are less important to ribosomal function are less likely
> > to be transferred and preserved according to the probabilities of
> > natural selection.
>
> Why?
I conjecture that the genes that are more vital for ribosomal function
have a higher relative fitness compared to the genes that are less
vital for ribosomal function. And relative fitness corresponds to the
percent of selective advantage. And the percent of selective advantage
corresponds to the probability of fixation by postive natural
selection. So if a mutation puts a mitochondrial gene into the nuclear
genome, then the selective advantage of the given gene determines the
probability of fixation for that gene. Likewise, the vitalness of the
gene function corresponds to the probability of fixation for the
respective gene. (I hope that I made myself clear, but I will try again
if I am still unclear.)
By the way, Buratovich orignally proposed that front-loaded ID caused
the hierarchal rps gene transfer. But in a Letter to the Editor, I
(December, 2005) proposed that the probabilities of natural selection
can explain the hierarchy. And Buratovich personally conceded to me,
"With respect to selection and mutations being solely responsible for
the hierarchy, I must admit that this is wholly possible."
Larry Moran
John Wilkins <jo...@wilkins.id.au> wrote:
[snip]
> Not really. It was off-the-cuff. But if mtDNA lacks "junk" (whatever that is)
> it might be because the functions of "junk" DNA, such as producing miRNAs to
> regulate expression of "non-junk" DNA, has been shifted to the nuclear genome.
John, John, John, .... for a philosopher you sure get yourself into some
horrible semantic muddles.
Junk DNA does not have a function. That's what "junk" means.
miRNA is mostly wishful thinking.
Larry Moran
Friar Broccoli
Larry Moran wrote:
> John, John, John, .... for a philosopher you sure get yourself into some
> horrible semantic muddles.
This implies that philosophy sometimes clarifies issues.
What discipline did you intend to refer to?
Cordially
Friar Broccoli
Robert Keith Elias, Quebec, Canada Email: EliasRK (of) gmail * com
Best programmer's & all purpose text editor: http://www.semware.com
--------- I consider ALL arguments in support of my views ---------
John Harshman
> Greetings John,
> I have two thoughts here. 1) Are mitochondria subject to increased
> selection pressure because they are competing amongst themselves within
> the cell?,
Don't quite know what "increased selection pressure" would mean here,
but there is clearly selection among mitochondria within a cell. And
selection might favor faster replication. Or it might not.
> and 2) could there be some error-check mechanism in the
> nuclear genome that reduces mitochondrial mutations or cause apoptosis
> in mutant mitos?
Highly doubtful.
John Harshman
> John Harshman wrote:
>
>>rev.goetz wrote:
[snip]
>>>>>Yes, no natural selection is required. Neutral theory helps to explain
>>>>>this. On the other hand, the hierarchal transfer of ribosomal protein
>>>>>small unit (_rps_) genes from mitochondrial genomes to nuclear genomes
>>>>>most likely resulted from natural selection because the hierarchy
>>>>>relates to the importance on the functional importance of respective
>>>>>the _rps_ genes.
>>>>>
>>>>
>>>>Words missing or added here? It doesn't parse. Not sure what you mean by
>>>>"hierarchal transfer" either. At any rate, plase explain why rps
>>>>transfer to the nucleus is any less potentially the result of neutral
>>>>processes than, say, cytochrome c transfer.
>>>
>>>
>>>I do not know enough about cytochrome c to make the comparison, but I
>>>will try to explain the hierarchy and the relationship to natural
>>>selection. Buratovich (2005) notes an approximate hierarchy in the
>>>transfer of rps genes from the mitochondrial genome to the nuclear
>>>genome based on a comparison of 14 species. The approximate hierarchy
>>>follows: rps1, rps10, rps11, rps2, rps7, rps8, rps4, rps19, rps19,
>>>rps13, rps14, rps12, and rps3.
>>
>>Still not clear what "hierarchy" means here. Do you mean that there is
>>an ordering to the probability of transfer, with one end high and the
>>other end low? Or that transfer of one gene on the list is a
>>prerequisite for transfer of the next? Or what?
>
> The hierarchy includes both the historical sequence of the transfer and
> the probability of the transfer. The sequence, however, is not a
> prerequisite, but a typical order with occasional exceptions.
You have amazing powers of non-clarity.
>>>The genes that encode the proteins that are more vital for ribosomal
>>>function are more likely to be transferred and preserved according to
>>>the probabilities of natural selection. Likewise, the genes that encode
>>>proteins that are less important to ribosomal function are less likely
>>>to be transferred and preserved according to the probabilities of
>>>natural selection.
>>
>>Why?
>
> I conjecture that the genes that are more vital for ribosomal function
> have a higher relative fitness compared to the genes that are less
> vital for ribosomal function.
This makes no sense in standard biological terms. Loci are not competing
between each other and have no relative fitnesses in any usual sense.
Perhaps you mean it in some non-usual sense, but I don't know what you mean.
> And relative fitness corresponds to the
> percent of selective advantage. And the percent of selective advantage
> corresponds to the probability of fixation by postive natural
> selection. So if a mutation puts a mitochondrial gene into the nuclear
> genome, then the selective advantage of the given gene determines the
> probability of fixation for that gene. Likewise, the vitalness of the
> gene function corresponds to the probability of fixation for the
> respective gene. (I hope that I made myself clear, but I will try again
> if I am still unclear.)
This is relatively clear, but highly confused. What is the advantage to
the organism or to the mitochondrion if a given gene is in the nucleus
or mt genome? What is driving the nuclear copy to fixation and the mt
copy to extinction? Why should the vitalness of a gene change that
advantage, whatever it is?
> By the way, Buratovich orignally proposed that front-loaded ID caused
> the hierarchal rps gene transfer. But in a Letter to the Editor, I
> (December, 2005) proposed that the probabilities of natural selection
> can explain the hierarchy. And Buratovich personally conceded to me,
> "With respect to selection and mutations being solely responsible for
> the hierarchy, I must admit that this is wholly possible."
And I still don't understand what this hierarchy is. Step back a bit.
What are the raw data that are being interpreted here? Are you looking
at lists of species with particular genes either in mt or nuclear
genomes? Are you looking at phylogenetic trees with gene transfers
mapped onto them? Or something else?
>>Buratovich (June 2005) _Perspectives on Science and Christian Faith_.
>>Table 2, p.107.
Could you give a complete citation for this, just in case I can locate
it somewhere? Author's full name, article's title, page numbers, etc.
Matt Silberstein
<Eli...@gmail.com> in
<1136474117....@g47g2000cwa.googlegroups.com> wrote:
>
>Larry Moran wrote:
>
>
>> John, John, John, .... for a philosopher you sure get yourself into some
>> horrible semantic muddles.
>
>This implies that philosophy sometimes clarifies issues.
>What discipline did you intend to refer to?
>
Read _Metaphysics of Evolution_ or _Science as a Process_, both by
David Hull.
rev.goetz
Most of the rps genes transferred from the mitochondial genome to the
nuclear genome in several lineages. And the genes were conserved after
the transfer, and they currently perform vital ribosomal functions.
Since the genes were conserved after the transfer and they currently
perfom vital functions, I conjecture that the transfer was caused by
natural selection as opposed to random drift. On the other hand, I do
not have the slightest idea why the transfer had a selective
andvantage.
If you want more details about the history of the rps gene transfers,
you will have to look up the Buratovich (2005) article and its
respective references.
Buratovich, Michael. "The Serial Endosymbiosis Theory: Cellular
Origins and Intelligent Design Theory," _Perspective on Science and
Christian Faith_, 57:2, p. 98-1??, June 2005.
Below is a link to a list of libraries that carry _Perspective on
Science and Christian Faith_:
http://www.asa3.org/ASA/asalib.html
John Harshman
In a particular order?
> And the genes were conserved after
> the transfer, and they currently perform vital ribosomal functions.
Well, duh.
> Since the genes were conserved after the transfer and they currently
> perfom vital functions, I conjecture that the transfer was caused by
> natural selection as opposed to random drift. On the other hand, I do
> not have the slightest idea why the transfer had a selective
> andvantage.
Sorry, this makes no sense. We're talking about the transfer. Of course
the genes are conserved by selection. All functional genes are conserved
by selection. If there are two copies, it's likely that only one of them
will be conserved, which accounts for loss of the mitochondrial copy.
(Note that even if we flip a coin to see which copy is conserved after
any duplication event, the mitochondrion will progressively lose genes,
since there is no force copying nuclear-encoded mt genes back into the
mt genome. If, by chance, the mt copy is lost, that's it. If the nuclear
copy is lost, we never hear about it. We will sometimes see nuclear
mt-pseudogenes, and we do.)
Don't confuse the forces maintaining the existence of at least one
functional copy with the forces that cause transfer of genes to the
nucleus (which includes two steps: 1) copying; 2) loss of the mt copy).
> If you want more details about the history of the rps gene transfers,
> you will have to look up the Buratovich (2005) article and its
> respective references.
>
> Buratovich, Michael. "The Serial Endosymbiosis Theory: Cellular
> Origins and Intelligent Design Theory," _Perspective on Science and
> Christian Faith_, 57:2, p. 98-1??, June 2005.
>
> Below is a link to a list of libraries that carry _Perspective on
> Science and Christian Faith_:
> http://www.asa3.org/ASA/asalib.html
I don't suppose this is online anywhere that you know of? I see there is
a library near me, and I may try it. Interesting that Buratovich is (or
at least once was) on the NCSE advisory board. Based on press releases
from his sectarian college, his argument seems like a seriously naive
misunderstanding of Darwinian theory, i.e. his claim that natural
selection explains only competition, never cooperation.
rev.goetz
There was a typical order with occasional exceptions. I already gave
you the order: "The approximate hierarchy follows: rps1, rps10, rps11,
rps2, rps7, rps8, rps4, rps19, rps19, rps13, rps14, rps12, and rps3."
>
> > And the genes were conserved after
> > the transfer, and they currently perform vital ribosomal functions.
>
> Well, duh.
>
> > Since the genes were conserved after the transfer and they currently
> > perfom vital functions, I conjecture that the transfer was caused by
> > natural selection as opposed to random drift. On the other hand, I do
> > not have the slightest idea why the transfer had a selective
> > andvantage.
>
> Sorry, this makes no sense. We're talking about the transfer. Of course
> the genes are conserved by selection. All functional genes are conserved
> by selection. If there are two copies, it's likely that only one of them
> will be conserved, which accounts for loss of the mitochondrial copy.
> (Note that even if we flip a coin to see which copy is conserved after
> any duplication event, the mitochondrion will progressively lose genes,
> since there is no force copying nuclear-encoded mt genes back into the
> mt genome. If, by chance, the mt copy is lost, that's it. If the nuclear
> copy is lost, we never hear about it. We will sometimes see nuclear
> mt-pseudogenes, and we do.)
>
> Don't confuse the forces maintaining the existence of at least one
> functional copy with the forces that cause transfer of genes to the
> nucleus (which includes two steps: 1) copying; 2) loss of the mt copy).
Okay, I conjecture that the duplication in the nuclear genome was
preserved by natural selection since the original mutation event. And
the loss of the mt copy could have been drift or selection. However, if
the mt copy was lost by drift, the lack of selection on the mt copy
occurred only because of the selection preserving the nuclear copy. So
even if drift was involved, natural selection was still a factor.
>
> > If you want more details about the history of the rps gene transfers,
> > you will have to look up the Buratovich (2005) article and its
> > respective references.
> >
> > Buratovich, Michael. "The Serial Endosymbiosis Theory: Cellular
> > Origins and Intelligent Design Theory," _Perspective on Science and
> > Christian Faith_, 57:2, p. 98-1??, June 2005.
> >
> > Below is a link to a list of libraries that carry _Perspective on
> > Science and Christian Faith_:
> > http://www.asa3.org/ASA/asalib.html
>
> I don't suppose this is online anywhere that you know of? I see there is
> a library near me, and I may try it. Interesting that Buratovich is (or
> at least once was) on the NCSE advisory board. Based on press releases
> from his sectarian college, his argument seems like a seriously naive
> misunderstanding of Darwinian theory, i.e. his claim that natural
> selection explains only competition, never cooperation.
I know that the journal publishes all articles online after roughly 2
years. But I do not know of an online source in the meantime.
I agree with you that his argument is weak. In personal communication,
I refuted Buratovich on 2 points. First, I refuted his claim that the
rps hierarchy resulted from ID instead on natural selection. Second,
his article does not credit Darwin for Darwin's discussions of
co-evolution, which I think has some similarity to endosymbiosis, at
least conceptually. But my Letter to the Editor (December, 2005)
included only the first point.
On the other hand, the article gave me an excellent review of
endosymbiosis theory.
John Wilkins
the use-mention distinction, but "scare quotes" might have given you the idea
that I don't think it is all "junk"...
As to miRNAs, people who seem to know what they are talking about think they
are real. If you disagree, I'm sure that will be fought out in the journals...
John Harshman
Don't confuse order with hierarchy. And don't confuse me by confusing
them. OK, so that's the order. Now, how did the author figure out the
order? It would be necessary for some species to exist with all possible
intermediate states, i.e. all except rps3 transferred to the nucleus,
all except rps12 and rps3 transferred, etc., and all the taxa with those
conditions arranged as subsets with the proper nesting. Is that the case?
Yes, yes. Natural selection preserves one copy. Drift disposes of the
other. This is not in dispute. The point is that natural selection does
*not* explain the transfer of function to the nucleus. Nor does it
explain in any way why there should be an order to the transfer of rps
genes. Or at least you have not proposed any explanation so far.
>>>If you want more details about the history of the rps gene transfers,
>>>you will have to look up the Buratovich (2005) article and its
>>>respective references.
>>>
>>>Buratovich, Michael. "The Serial Endosymbiosis Theory: Cellular
>>>Origins and Intelligent Design Theory," _Perspective on Science and
>>>Christian Faith_, 57:2, p. 98-1??, June 2005.
>>>
>>>Below is a link to a list of libraries that carry _Perspective on
>>>Science and Christian Faith_:
>>>http://www.asa3.org/ASA/asalib.html
>>
>>I don't suppose this is online anywhere that you know of? I see there is
>>a library near me, and I may try it. Interesting that Buratovich is (or
>>at least once was) on the NCSE advisory board. Based on press releases
>>from his sectarian college, his argument seems like a seriously naive
>>misunderstanding of Darwinian theory, i.e. his claim that natural
>>selection explains only competition, never cooperation.
>
> I know that the journal publishes all articles online after roughly 2
> years. But I do not know of an online source in the meantime.
>
> I agree with you that his argument is weak. In personal communication,
> I refuted Buratovich on 2 points. First, I refuted his claim that the
> rps hierarchy resulted from ID instead on natural selection. Second,
> his article does not credit Darwin for Darwin's discussions of
> co-evolution, which I think has some similarity to endosymbiosis, at
> least conceptually. But my Letter to the Editor (December, 2005)
> included only the first point.
Endosymbiosis is one form of co-evolution.
Steve Schaffner
> rev.goetz wrote:
> >
> > There was a typical order with occasional exceptions. I already gave
> > you the order: "The approximate hierarchy follows: rps1, rps10, rps11,
> > rps2, rps7, rps8, rps4, rps19, rps19, rps13, rps14, rps12, and rps3."
>
> Don't confuse order with hierarchy. And don't confuse me by confusing
> them. OK, so that's the order. Now, how did the author figure out the
> order? It would be necessary for some species to exist with all possible
> intermediate states, i.e. all except rps3 transferred to the nucleus,
> all except rps12 and rps3 transferred, etc., and all the taxa with those
> conditions arranged as subsets with the proper nesting. Is that the case?
[...]
>
> Yes, yes. Natural selection preserves one copy. Drift disposes of the
> other. This is not in dispute. The point is that natural selection does
> *not* explain the transfer of function to the nucleus. Nor does it
> explain in any way why there should be an order to the transfer of rps
> genes. Or at least you have not proposed any explanation so far.
My first thought was that the order (if it is a real effect) would
correlate with transcript abundance, but this does not seem consistent
with the evidence (Genome Research, Vol. 12, Issue 6, 885-893, June
2002). My second guess would be varying recombination rates at
different points in the mtDNA sequence. My zeroeth guess would be
that the order is an artifact.
--
Steve Schaffner s...@broad.mit.edu
Immediate assurance is an excellent sign of probable lack of
insight into the topic. Josiah Royce
Ron O
Dale wrote:
> "John Harshman" <jharshman....@pacbell.net> wrote in message
> news:otEuf.6229$UF3....@newssvr25.news.prodigy.net...
> > Selection for fast replication? That's the usual idea for bacteria, but
> > do mitochondria have to replicate that often compared to the nucleus of
> > the same cell? That would depend on the lifetime of a mitochondrion and
> > its standing population in the cell. I'll have to look that up.
> >
> > If not that, then what?
> >
> > There are mitochondria with junk. In fact the control region has been
> > duplicated several times in different groups of birds, and one of the
> > copies is clearly non-functional. So it does happen. But why so rarely?
>
> up some DNA in favor of a symbiotic relationship?
>
> And consider if mutated junk DNA has anything to do with phenotype. If a
> mitochondrion had some junk DNA, and then there were a mutation that
> activated the junk and made it non-junk, then it might become more like an
> invader than a symbiont. So anything that had mitochondria with a lot of
> junk would have a tendency to die a horrible death, and then of course that
> would be the end of the line for that mitochondrial "species".
>
> Okay, I'm just pulling stuff out of my ass here, I've been reading a
> textbook on molecular cell biology, but maybe there's something there that
> can help.
As a grad student I wrote a paper on repetitive DNA in nematode
mitochondria. Copy number varied between closely related species.
Some had quite a bit of the repeats, but I don't know if it had any
function. It was a short repeat like satelite DNA. C. elegans had a
dinucleotide microsatellite in its mitochonrial genome.
Ron Okimoto
John Harshman
How many repeats, on average? Are we talking significant amounts of
sequence? Were these in intergenic spacers, control region (if nematodes
have a control region), or something else?
John Harshman
> John Harshman <jharshman....@pacbell.net> writes:
>
>
>>rev.goetz wrote:
>>
>>>There was a typical order with occasional exceptions. I already gave
>>>you the order: "The approximate hierarchy follows: rps1, rps10, rps11,
>>>rps2, rps7, rps8, rps4, rps19, rps19, rps13, rps14, rps12, and rps3."
>>
>>Don't confuse order with hierarchy. And don't confuse me by confusing
>>them. OK, so that's the order. Now, how did the author figure out the
>>order? It would be necessary for some species to exist with all possible
>>intermediate states, i.e. all except rps3 transferred to the nucleus,
>>all except rps12 and rps3 transferred, etc., and all the taxa with those
>>conditions arranged as subsets with the proper nesting. Is that the case?
>
> [...]
>
>>Yes, yes. Natural selection preserves one copy. Drift disposes of the
>>other. This is not in dispute. The point is that natural selection does
>>*not* explain the transfer of function to the nucleus. Nor does it
>>explain in any way why there should be an order to the transfer of rps
>>genes. Or at least you have not proposed any explanation so far.
>
>
> My first thought was that the order (if it is a real effect) would
> correlate with transcript abundance, but this does not seem consistent
> with the evidence (Genome Research, Vol. 12, Issue 6, 885-893, June
> 2002).
Meaning the evidence that the transfer is not RNA-mediated? Also, I
don't think there is such a thing as transcript abundance. Isn't the
mitochondrion transcribed as a unit?
> My second guess would be varying recombination rates at
> different points in the mtDNA sequence.
Recombination? Why recombination? I'd be interested to know if the
transfer frequency correlates negatively with distance from the origin
of replication. Are the human pseudogenes biased in distribution in any
way? I see the size distribution is quite wide.
> My zeroeth guess would be
> that the order is an artifact.
Presumably there is some literature on this somewhere. I doubt that any
primary results are being published in Christian apologetics magazines.
rev.goetz
I think that you are accurately describing the data. Buratovich has a
rich bibliography with dozens of references. While I disagree with his
conclusions about ID, I recommend the review sections of his article.
Here is one of his primary references: Lang BF, Gray MW, Burger G.,
"Mitochondrial genome evolution and the origin of eukaryotes"
_Annu_ _Rev_ _Genet_ (1999) 33:351-97.
Buratovich (June, 2005: p. 109) notes that the typical order of the
gene transfers correspond to the importance of each respective nuclear
gene function in regards to the ribosome. And I (December, 2005)
conjecture that the various levels of importance for each nuclear gene
correspond to various levels of selective advantage for each nuclear
gene. And this helps to explain how natural selection caused the
typical order of the gene transfers.
On the other hand, I have no clue as to why in various lineages say the
nuclear rps1 had a significant positive selective advantage while the
mt rps1 was not preserved by natural selection. Perhaps an extensive
literature review would answer that question for me, but for now I do
not have the time to do such a literature review.
John Harshman
Thanks for that reference.
No it doesn't. Unless there is an advantage to the transfer itself,
natural selection doesn't explain it. The importance of the gene has
nothing to do with this. The importance (or lack thereof) of the
*location* of the gene is what you need to explain. If there is indeed
an ordering of transfers by importance, you have so far not managed to
connect that phenomenon with any explanation. You supposed explanation
is empty.
> On the other hand, I have no clue as to why in various lineages say the
> nuclear rps1 had a significant positive selective advantage while the
> mt rps1 was not preserved by natural selection. Perhaps an extensive
> literature review would answer that question for me, but for now I do
> not have the time to do such a literature review.
Actually, I can think of a reason why there might actually be a bias
toward preservation of the nuclear copy. However, this bias has no
relationship to the importances of the genes. If, during the period
when two functional copies exist, one of the genes experiences a loss of
function mutation, the other one will take over and the other will no
longer be subject to selection. mtDNA has a much higher mutation rate
than nDNA (in most metazoans, at least -- not true throughout life) and
therefore the mt copy is more likely to experience that first loss of
function mutation. Interestingly, green plants have a much slower rate
of mtDNA than nDNA evolution, and I seem to recall that their mt genomes
are unusually large. Coincidence? Don't know.
[snip]
Steve Schaffner
> Steve Schaffner wrote:
>
> > John Harshman <jharshman....@pacbell.net> writes:
> >
> >
> >>rev.goetz wrote:
> >>
> >>>There was a typical order with occasional exceptions. I already gave
> >>>you the order: "The approximate hierarchy follows: rps1, rps10, rps11,
> >>>rps2, rps7, rps8, rps4, rps19, rps19, rps13, rps14, rps12, and rps3."
> >>
> >>Don't confuse order with hierarchy. And don't confuse me by confusing
> >>them. OK, so that's the order. Now, how did the author figure out the
> >>order? It would be necessary for some species to exist with all possible
> >>intermediate states, i.e. all except rps3 transferred to the nucleus,
> >>all except rps12 and rps3 transferred, etc., and all the taxa with those
> >>conditions arranged as subsets with the proper nesting. Is that the case?
> >
> > [...]
> >
> >>Yes, yes. Natural selection preserves one copy. Drift disposes of the
> >>other. This is not in dispute. The point is that natural selection does
> >>*not* explain the transfer of function to the nucleus. Nor does it
> >>explain in any way why there should be an order to the transfer of rps
> >>genes. Or at least you have not proposed any explanation so far.
> >
> >
> > My first thought was that the order (if it is a real effect) would
> > correlate with transcript abundance, but this does not seem consistent
> > with the evidence (Genome Research, Vol. 12, Issue 6, 885-893, June
> > 2002).
>
> Meaning the evidence that the transfer is not RNA-mediated?
Yes. Among other pieces of evidence, the presence of copies of
nontranscribed mtDNA in the nuclear genome.
> Also, I
> don't think there is such a thing as transcript abundance. Isn't the
> mitochondrion transcribed as a unit?
I think it is more than one transcription unit, and in any case
they're broken down into single-gene segments. (And abundance depends
both on production rate and on how long each one lasts.) But I don't
know much about mtDNA, and my first reactions were wild guesses.
> > My second guess would be varying recombination rates at
> > different points in the mtDNA sequence.
>
> Recombination? Why recombination?
Nonhomologous recombination with a nuclear chromosome. Some mtDNA
sites might be more prone that way.
I'd be interested to know if the
> transfer frequency correlates negatively with distance from the origin
> of replication. Are the human pseudogenes biased in distribution in any
> way? I see the size distribution is quite wide.
>
> > My zeroeth guess would be
> > that the order is an artifact.
>
> Presumably there is some literature on this somewhere. I doubt that any
> primary results are being published in Christian apologetics magazines.
--
rev.goetz
Do you think that the importance of the gene could correspond to the
probability of fixation for the duplication in the nuclear genome?
John Harshman
I see no reason why it should. Do you?
rev.goetz
Well, I think that the importance of a gene corresponds to the relative
fitness of the gene after gene duplication.
Could genes with ribosomal function have more importance to the nuclear
genome as compared to the mitochondrial genome?
Ron O
In C. elegans we called the putative control region (around 500 bp) the
AT region because there is very little GC in it. It has around a 30 bp
AT microsatellite with a half dozen 40 bp repeats in it.
Meloidogyne species have a 102 bp and a 63 bp repeat in the putative
control region. We sequenced javanica and it had around 30 copies of
the 102 bp repeat (we couldn't sequence through the entire repeat
because it was too long and most of the repeats were identical and it
was over 3 kb), 5 copies of an 8 bp repeat, and 11 copies of a 63 bp
repeat.
I could look up the references in my CV if you want it.
Ron Okimoto
Larry Moran
Larry Moran
> John Harshman wrote:
>> rev.goetz wrote:
>> > John Harshman wrote:
>> >>rev.goetz wrote:
[snip]
>> >>>>Buratovich (June 2005) _Perspectives on Science and Christian Faith_.
>> >>>>Table 2, p.107.
>> >>
>> >>Could you give a complete citation for this, just in case I can locate
>> >>it somewhere? Author's full name, article's title, page numbers, etc.
>> >
>> > Most of the rps genes transferred from the mitochondial genome to the
>> > nuclear genome in several lineages.
>>
>> In a particular order?
>
> There was a typical order with occasional exceptions. I already gave
> you the order: "The approximate hierarchy follows: rps1, rps10, rps11,
> rps2, rps7, rps8, rps4, rps19, rps19, rps13, rps14, rps12, and rps3."
The numbers refer to the transfer of ribosomal protein genes from the
mitochondrial geneome to the nucleus in flowering plants. Genes that
are labelled "rps" refer to small subunit genes while genes labelled
"rpl" refer to large subunit genes.
Adams et al. (2002) looked at 280 different species of angiosperms.
Adams, K.L., Qiudagger, Y-L., Stoutemyer, M. and
Palmer, J.D. (2002) Punctuated evolution of mitochondrial
gene content: High and variable rates of mitochondrial
gene loss and transfer to the nucleus during angiosperm
evolution. PNAS 99,9905-9912.
They found that the transfer of these genes was highly variable. Here
are the total number of times that each gene has been transferred to
the nucleus.
rpl2 41
rpl5 19
rpl16 15
rps1 33
rps2 8
rsp3 7
rps4 7
rps7 41
rps10 26
rps11 14
rps12 6
rps13 30
rps14 27
rps19 39
Some genes are transferred more often than others although the hierarchy
differs from that suggested by Buratovich. Adams et al. (2002) don't offer
a specific explanation of this hierarchy although they suggest that it
reflects gene specific factors ...
"Among ribosomal protein genes, all of which have been lost
relatively frequently in angiosperms, there nonetheless seems
to be a gradient/hierachy with respect to likelihood of
transfer, both within angiosperms (Table 1) and on the broad
scale of eukaryotic evolution. As with respiratory genes, this
gradient is likely to reflect a gene- and lineage-specific
interplay of multiple factors."
One of those factors has to do with the ease of import into mitochondria.
All of the genes that are transferred to the nucleus have to acquire an
mitochondrial import signal before the protein can find it's way back into
the mitochondria. In some cases all you have to do is tack on an N-terminal
mitochondrial import signal from another gene and the protein will easily
go into the mitochondria.
In other cases, the basic ribosomal protein may not be compatible with the
mitochondrial import apparatus so further modifications are necessary
before a transfer is successful. Proteins have to be unfolded during
transfer across the mitochondrial membrane then refolded under the
influence of mitochondrial chaperones once they reach the internal
mitochondrial matrix. Some proteins are better preadapted to this than
others.
Larry Moran
Larry Moran
> John Harshman wrote:
>> rev.goetz wrote:
[snip]
>> > Do you think that the importance of the gene could correspond to the
>> > probability of fixation for the duplication in the nuclear genome?
>>
>> I see no reason why it should. Do you?
>
> Well, I think that the importance of a gene corresponds to the relative
> fitness of the gene after gene duplication.
>
> Could genes with ribosomal function have more importance to the nuclear
> genome as compared to the mitochondrial genome?
Read this paper for a discussion of the various explanations for transfer
to the nucleus.
Adams, K.L. and Palmer, J.D. (2003) Evolution of mitochondrial
gene content: gene loss and transfer to the nucleus.
Molecular Phylogenetics and Evolution 29, 380-395
1. Introduction
2. Evolution of mitochondrial gene content
2.1. Ribosomal RNA genes
2.2. Transfer RNA genes
2.3. Protein genes葉he big picture
2.4. Protein genes in plantså‚oth stasis and lots of action
2.5. Mitochondria without a genome
3. Why mitochondrial gene loss?
4. Transfer of mitochondrial genes to the nucleus
4.1. Mitochondrial pseudogenes in the nucleus
4.2. Gene escape, transfer, and integration into nuclear DNA
4.3. Activation and expression of a transferred gene
4.4. Split gene transfers
4.5. Frequency of functional mitochondrial gene transfer
5. Factors promoting or retarding gene transfer
5.1. Is gene transfer a selective or neutral process?
5.2. Why do mitochondria retain genomes?
5.3. Are nuclear genes transferred back to mitochondria?
Section 5.1 is my favorite.
Larry Moran
John Harshman
No, thanks, that was good enough. 3 kb is enough to make what I would
consider a significant difference in genome size. I'm assuming the
mean/default genome size in nematodes isn't much different from that in
vertebrates, i.e. around 16kb.
John Harshman
> John Harshman wrote:
>
>>rev.goetz wrote:
[snip]
>>>Do you think that the importance of the gene could correspond to the
>>>probability of fixation for the duplication in the nuclear genome?
>>
>>I see no reason why it should. Do you?
>
> Well, I think that the importance of a gene corresponds to the relative
> fitness of the gene after gene duplication.
Genes don't have fitnesses. Alleles do. Now we could talk about
differences in fitness between a duplicated gene (mt and nuclear copies)
and an unduplicated gene (mt copy only), if that's what you mean. I
don't see why we would expect such a difference, though.
> Could genes with ribosomal function have more importance to the nuclear
> genome as compared to the mitochondrial genome?
No, since the genes in question are specific to mitochondrial ribosomes.
Eukaryotic ribosomes need a whole different set of ribosomal proteins,
coded for by different nuclear genes.
John Harshman
Care to the summarize the take-home message?
rev.goetz
Larry Moran wrote:
> On 5 Jan 2006 21:21:28 -0800, rev.goetz <jimgo...@yahoo.com> wrote:
> > John Harshman wrote:
> >> rev.goetz wrote:
>
> [snip]
>
> >> > Do you think that the importance of the gene could correspond to the
> >> > probability of fixation for the duplication in the nuclear genome?
> >>
> >> I see no reason why it should. Do you?
> >
> > Well, I think that the importance of a gene corresponds to the relative
> > fitness of the gene after gene duplication.
> >
> > Could genes with ribosomal function have more importance to the nuclear
> > genome as compared to the mitochondrial genome?
>
> Read this paper for a discussion of the various explanations for transfer
> to the nucleus.
>
> Adams, K.L. and Palmer, J.D. (2003) Evolution of mitochondrial
> gene content: gene loss and transfer to the nucleus.
> Molecular Phylogenetics and Evolution 29, 380-395
>
> 1. Introduction
> 2. Evolution of mitochondrial gene content
> 2.1. Ribosomal RNA genes
> 2.2. Transfer RNA genes
> 2.4. Protein genes in plants-both stasis and lots of action
> 2.5. Mitochondria without a genome
> 3. Why mitochondrial gene loss?
> 4. Transfer of mitochondrial genes to the nucleus
> 4.1. Mitochondrial pseudogenes in the nucleus
> 4.2. Gene escape, transfer, and integration into nuclear DNA
> 4.3. Activation and expression of a transferred gene
> 4.4. Split gene transfers
> 4.5. Frequency of functional mitochondrial gene transfer
> 5. Factors promoting or retarding gene transfer
> 5.1. Is gene transfer a selective or neutral process?
> 5.2. Why do mitochondria retain genomes?
> 5.3. Are nuclear genes transferred back to mitochondria?
>
> Section 5.1 is my favorite.
>
>
> Larry Moran
Excellent article, and the author makes it available on his university
webpage.
r norman
wrote:
And the link to which you should have included in your message
http://www.bio.indiana.edu/%7Epalmerlab/Website/Journals/Journals/197.pdf
rev.goetz
> rev.goetz wrote:
>
> > John Harshman wrote:
> >
> >>rev.goetz wrote:
>
> [snip]
>
> >>>Do you think that the importance of the gene could correspond to the
> >>>probability of fixation for the duplication in the nuclear genome?
> >>
> >>I see no reason why it should. Do you?
> >
> > Well, I think that the importance of a gene corresponds to the relative
> > fitness of the gene after gene duplication.
>
> Genes don't have fitnesses. Alleles do. Now we could talk about
> differences in fitness between a duplicated gene (mt and nuclear copies)
> and an unduplicated gene (mt copy only), if that's what you mean. I
> don't see why we would expect such a difference, though.
Okay, I am referring the initial mutational event of the mt gene
inserting into the nuclear genome of an individual specimen. That
initial mutational event resulted in essentially a new allele in the
nuclear genome. Instead of using the term "fitness, we will say that
the new allele had an advantage that was positive or neutral or
negative. And the new allele either became fixed or became extinct. And
in most cases the new allele became extinct. But in some cases, the new
allele fixed in the nuclear genome. And if the new allele had a
positive advantage, the new allele fixed by natural selection.
So I will say that the importance of the allele corrosponds to the
advantage of allele.
Ron O
It is actually smaller, less than 15 kb needed. All the genes are
smaller including the tRNAs that are missing one arm.
Ron Okimoto
John Harshman
The question to ask is why there should be such an advantage.
rev.goetz
Your question sounds deeply philosophical and beyond the realm of
science. Science cannot answer questions about why should there be
anything.
Or did you mean say that the question to ask is why there was such an
advantage?
John Harshman
"Why" has several meanings, and the teleological meaning is irrelevant
here. Note that you yourself use "why" in your question. This is a red
herring.
In order to ask why there was such an advantage, we have to establish
that there indeed was such an advantage, which you have not done. I was
asking for a theoretical reason why there would have been such an
advantage. If we can come up with a plausible reason, we have made progress.
rev.goetz
I was not suggesting anything teleological about the use of the word
"why." But your phrase "why should" was confusing, enough with that.
Apart from any knowledge of gene function, we know that there was a
molecular convergence of homologues in several lineages where
functional rps genes duplicated and were conserved for hundreds of
millions of years. It would be hard for me to imagine if this resulted
from drift. This looks like selection to me, at least in the cases of
the duplicated functioning genes that were conserved for hundreds of
millions of years.
As I stated earlier, there is a proposed rps gene hierarchy related to
the importance of each gene in regards to the function of the ribosome.
For example, rps1 is high in importance to the ribosome, where the
ribosomal protein S1 has RNA unwinding activity, helps the binding of
mRNA to the ribosome, and influences the affinity of ribosomes for
different mRNA initiation sequences.
If indeed there is a rps gene hierarchy related to the importance of
each gene in regards to the function of the ribosome, then that
hierarchy may correspond to a hierarchy of selective advantage. And so
far you have not shown me any reason why a hierarchy of gene function
importance would not correspond to a hierarchy of selective advantage.
John Harshman
You remain seriously confused, and this is reflected in your ambiguous
language. By "molecular convergence of homologues" you appear to mean
that the same genes were transferred from mitochondrial to nuclear
genome several times. "And were conserved" seems to mean that the genes,
once transferred, remained under purifying selection. But that has
nothing to do with transfer, only with conservation of a functional
product, wherever its coding gene happens to be located. Again, nobody
is arguing that functional genes were not preserved by selection. The
question is whether there is any reason to believe that the transfer of
those functional genes from mitochondrion to nucleus had anything to do
with selection. You have presented no reasons why we ought to think so,
nor have you suggested any possible mechanism of such selection.
> As I stated earlier, there is a proposed rps gene hierarchy related to
> the importance of each gene in regards to the function of the ribosome.
Hierarchy is a bad word to use here. What you mean is an ordering.
> For example, rps1 is high in importance to the ribosome, where the
> ribosomal protein S1 has RNA unwinding activity, helps the binding of
> mRNA to the ribosome, and influences the affinity of ribosomes for
> different mRNA initiation sequences.
>
> If indeed there is a rps gene hierarchy related to the importance of
> each gene in regards to the function of the ribosome, then that
> hierarchy may correspond to a hierarchy of selective advantage.
Selective advantage how? One gene doesn't have a selective advantage
over another. They aren't in competition. Increase in frequency of one
doesn't change the frequency of the other. This makes no sense unless
you have your own personal definition of selective advantage, different
from the standard one.
> And so
> far you have not shown me any reason why a hierarchy of gene function
> importance would not correspond to a hierarchy of selective advantage.
I have no idea what you would mean by that. More importantly, I have no
idea how this would relate to the matter at hand, transfer of genes from
mitochondrion to nucleus.
ErikW
> In message <pb7mr15p2cd59ur4g...@4ax.com>, r norman
> <NotMyRealEmail@_comcast.net> writes
> >
> >On another tack, why don't we hear about much about the chloroplast
> >genome? Is it just my chauvinistic animal kingdomism? Or that there
> >are too many cases of paternal inheritance -- all gymnosperms, for
> >example?
> >
> Botanists (at least the angiosperm/gymnosperm workers) do a lot more
> work with cpDNA than with mtDNA. About a score of complete embryophyte
> chloroplast genomes have been sequenced.
>
> BTW, chloroplast genomes have introns and, IIRC, other junk.
And plant mitochondria even more than chloroplasts, including
duplicated genes that makes mitochondria prone to intragenomic
recombination. That's also why most of the work is done with cpDNA in
plants.
In light of Larry Moran's post on Jan 4th, do plant mitochindria have a
different replication system than animal mitochondria?
ErikW
rev.goetz
You are distorting the context of my statements while you are ignoring
my previous posts on this topic from Jan 5 2006 7:19 pm and Jan 6 2006
5:51 pm. There would be no confusion about my statements if you stop
ignoring previous statements.
For example, Jan 5 2006 7:19 pm I wrote:
"Okay, I conjecture that the duplication in the nuclear genome was
preserved by natural selection since the original mutation event. And
the loss of the mt copy could have been drift or selection. However, if
the mt copy was lost by drift, the lack of selection on the mt copy
occurred only because of the selection preserving the nuclear copy. So
even if drift was involved, natural selection was still a factor."
And Jan 6 2006 5:51 pm I wrote:
"Okay, I am referring the initial mutational event of the mt gene
inserting into the nuclear genome of an individual specimen. That
initial mutational event resulted in essentially a new allele in the
nuclear genome. Instead of using the term 'fitness', we will say
that the new allele had an advantage that was positive or neutral or
negative. And the new allele either became fixed or became extinct. And
in most cases the new allele became extinct. But in some cases, the new
allele fixed in the nuclear genome. And if the new allele had a
positive advantage, the new allele fixed by natural selection."
If you would follow the context of my discussion, you would see that I
divide the gene transfer into two major steps: 1) the mutation and
fixation of the functioning gene duplication in the nuclear genome, 2)
the loss of the mt copy. And I conceded that the loss on the mt copy
may have resulted from drift. And if that was the case, then the loss
of the mt copy by drift depended upon natural selection preserving the
nuclear copy. This suggests that we have to only confirm evidence that
natural selection fixed and preserved the gene duplication in the
nuclear genome to show that natural selection was responsible for the
gene transfer.
And on my last post of this topic on Jan 8, I purposefully focused on
the evidence of natural selection in rps gene duplications that have
been preserved in the nuclear genome of several species for hundreds of
millions of years. The context for all of this should not confuse you.
John Harshman
I don't think so.
> For example, Jan 5 2006 7:19 pm I wrote:
> "Okay, I conjecture that the duplication in the nuclear genome was
> preserved by natural selection since the original mutation event. And
> the loss of the mt copy could have been drift or selection. However, if
> the mt copy was lost by drift, the lack of selection on the mt copy
> occurred only because of the selection preserving the nuclear copy. So
> even if drift was involved, natural selection was still a factor."
If that's all we're arguing about, I agree. Functional genes are
preserved by selection. If instead we are having some discussion about
why genes are transferred from the mitochondrion to the nucleus, this is
irrelevant.
> And Jan 6 2006 5:51 pm I wrote:
> "Okay, I am referring the initial mutational event of the mt gene
> inserting into the nuclear genome of an individual specimen. That
> initial mutational event resulted in essentially a new allele in the
> nuclear genome. Instead of using the term 'fitness', we will say
> that the new allele had an advantage that was positive or neutral or
> negative. And the new allele either became fixed or became extinct. And
> in most cases the new allele became extinct. But in some cases, the new
> allele fixed in the nuclear genome. And if the new allele had a
> positive advantage, the new allele fixed by natural selection."
So now I ask again: what might cause the new allele to become fixed by
natural selection? What advantage might it have? And again, we need to
be clear about what we mean by "allele". We are talking about one
"allele" in which there are two copies of the gene, one mitochondrial
and one nuclear, and the other allele had only a mitochondrial copy. I
think this is the step you are talking about here?
The second step might also involve selection, and here we are talking
about two different "alleles": one with both mt and nuclear copies, and
the other with a nuclear copy only.
Feel free to present reasons why any of these "alleles" might be
advantageous vs. the alternate allele.
> If you would follow the context of my discussion, you would see that I
> divide the gene transfer into two major steps: 1) the mutation and
> fixation of the functioning gene duplication in the nuclear genome, 2)
> the loss of the mt copy. And I conceded that the loss on the mt copy
> may have resulted from drift. And if that was the case, then the loss
> of the mt copy by drift depended upon natural selection preserving the
> nuclear copy. This suggests that we have to only confirm evidence that
> natural selection fixed and preserved the gene duplication in the
> nuclear genome to show that natural selection was responsible for the
> gene transfer.
>
> And on my last post of this topic on Jan 8, I purposefully focused on
> the evidence of natural selection in rps gene duplications that have
> been preserved in the nuclear genome of several species for hundreds of
> millions of years. The context for all of this should not confuse you.
But it does. You are presenting evidence for conservation of a
functional gene copy after all other copies have been lost, as if this
is at all relevant to the fixation of that gene in the presence of
another functional copy. But it isn't. And that's because you are
yourself confused about the event you are trying to explain. Once more,
you want to explain why, of the two genotypes below, the one on the left
might have an advantage:
Genotype A Genotype B
n-genome gene X -
mt-genome gene X gene X
Notice that it is no explanation to say that gene X is important; both
genotypes contain gene X. In fact, given that there are many
mitochondria in the average cell but only one nucleus, the difference in
copy number between genotypes must be negligible.
rev.goetz
Before I go further with this, I want to make sure that I understand
you on various points of the first major step of the gene transfer,
which is the fixation of the duplication in the nuclear genome. And
that you understand my definition of "allele." And I think that
your definition of "allele" is really should be used only for the
term "genotype."
I use a different definition of "allele" than you in the case of
gene transfer. I keep the concept of allele to apply to a single locus
while in the case of gene transfer there are two loci in two respective
genomes are involved. In the first step of the transfer, the new allele
is the duplication in nuclear genome. And in the case of rps1, the
first set of the transfer, the fixed duplication into the nuclear
genome occurred at least 33 times.
And you are saying that the preservation by natural selection for the
nuclear genome copy may have only occurred after the transfer was
completed. Is that correct? If I understand you correctly, you are
saying that rps1 may have fixed in the nuclear genome by drift in 33
separate occasions. Is that correct? (At this point, let us refrain
from talking about the complete gene transfer that by definition
includes the loss in the mt genome. We will get back to that later.)
John Harshman
> John Harshman wrote:
>
>>rev.goetz wrote:
>>
>>
>>>John Harshman wrote:
>>>
>>>
>>>>rev.goetz wrote:
[snip]
>>>And on my last post of this topic on Jan 8, I purposefully focused on
>>>the evidence of natural selection in rps gene duplications that have
>>>been preserved in the nuclear genome of several species for hundreds of
>>>millions of years. The context for all of this should not confuse you.
>>
>>But it does. You are presenting evidence for conservation of a
>>functional gene copy after all other copies have been lost, as if this
>>is at all relevant to the fixation of that gene in the presence of
>>another functional copy. But it isn't. And that's because you are
>>yourself confused about the event you are trying to explain. Once more,
>>you want to explain why, of the two genotypes below, the one on the left
>>might have an advantage:
>>
>> Genotype A Genotype B
>>n-genome gene X -
>>mt-genome gene X gene X
>>
>>Notice that it is no explanation to say that gene X is important; both
>>genotypes contain gene X. In fact, given that there are many
>>mitochondria in the average cell but only one nucleus, the difference in
>>copy number between genotypes must be negligible.
>
> Before I go further with this, I want to make sure that I understand
> you on various points of the first major step of the gene transfer,
> which is the fixation of the duplication in the nuclear genome. And
> that you understand my definition of "allele." And I think that
> your definition of "allele" is really should be used only for the
> term "genotype."
Whatever terms you like to use, I think that viewing this in terms of
genotypes with different copy numbers is the clearest way to do it. The
question you need to ask is why genotype A would be selected over
genotype B.
> I use a different definition of "allele" than you in the case of
> gene transfer. I keep the concept of allele to apply to a single locus
> while in the case of gene transfer there are two loci in two respective
> genomes are involved. In the first step of the transfer, the new allele
> is the duplication in nuclear genome. And in the case of rps1, the
> first set of the transfer, the fixed duplication into the nuclear
> genome occurred at least 33 times.
>
> And you are saying that the preservation by natural selection for the
> nuclear genome copy may have only occurred after the transfer was
> completed. Is that correct? If I understand you correctly, you are
> saying that rps1 may have fixed in the nuclear genome by drift in 33
> separate occasions. Is that correct? (At this point, let us refrain
> from talking about the complete gene transfer that by definition
> includes the loss in the mt genome. We will get back to that later.)
I'm asking you to provide any suggestion of a reason why the fixation of
a nuclear copy of rps1 might conceivably have been promoted by
selection. I'm not claiming that drift was responsible for that
fixation. I don't know. But at least drift is credible.
[snip]
rev.goetz
First, I will say that I doubt that drift is a credible explanation for
33 convergent duplications of a functioning gene, unless we see a
similar pattern of convergence with a gene sized chunk of
"nonconserved" DNA that duplicated from the mitochondrial genome to
the nuclear genome. And from what I have read, I do not here of such
convergence with nonconserved DNA. And I do not see how a statistical
model of neutral molecular evolution could possibly support such
convergence. Do you?
And if there was such an intense mutational pressure that mutated many
duplicate copies of a functioning gene from the mitochondrial genome to
the nuclear genome, then it would likely happen multiple times in the
same lineage. And at least in the case of plants, the rate mutation is
faster in the nuclear genome compared the mitochondrial genome, so if
everything in the gene transfer was neutral, then the greater amount of
mutations in the nuclear genome would more quickly silence the nuclear
copy, causing loss to the nuclear copy instead of the m copy .
Likewise, there would have to be numerous neutral duplications into the
nuclear genome before drift would cause the loss of the mitochondrial
copy. And from what I have read, there are few examples of multiple
duplications of functioning genes from the mitochondrial genome to the
nuclear genome within the same lineage. And I doubt that there are
enough such examples to defend a statistical model of neutral molecular
for duplications that occurred in over 30 lineages. Do you see such
evidence for a neutral model?
Concerning the advantage of what you call "genotype A" over
"genotype B," I saw a correlation for a proposed ranking of the
importance of the genes to the amount of times that it duplicated. This
may explain the advantage of genotype A over genotype B, but I now see
that it offers no explanation for the eventual loss of the m copy in
over 30 lineages. I clearly need to add something to my hypothesis. I
have more ideas on it after reading the article by Adams, K.L. and
Palmer, J.D. (2003) titles "Evolution of mitochondrial gene content:
gene loss and transfer to the nucleus," _Molecular_ _Phylogenetics_
_and_ _Evolution_ 29, 380-395. The article briefly reviews discusses
the potential buildup of deleterious mutations in the mitochondrial
genome. Now, such a buildup of deleterious mutations would not cause an
advantage for genotype A over genotype B, but such a buildup of
deleterious mutations would set up the nuclear copy for a rapid burst
of adaptive substitutions.
With all of this in mind, here is a possible scenario of gene transfers
that occurred in over 30 lineages. This scenario requires 3 major
steps: 1) the fixation of the duplication in the nuclear genome, 2) the
adaptive evolution of the nuclear copy, 3) the loss of the m copy to
drift. At first there was an advantage for more copies of the gene,
though that meant just two more copies in the nuclear genome, so this
led to the fixation of the duplication in nuclear genome. Then there
was a rapid burst of adaptive substitutions in the nuclear copy that
reversed a buildup of moderately deleterious substitutions that fixed
during the mitochondrial stage of the gene's ancestry. And this burst
of adaptation made the nuclear copy superior to the m copy so that
there was no more selective pressure to preserve the m copy. And the m
copy was eventually lost by drift to a silencing mutation.
>
> [snip]
John Harshman
There is no such DNA in the typical mitochondrion. Mitochondria tend to
have almost no junk DNA.
> And from what I have read, I do not here of such
> convergence with nonconserved DNA. And I do not see how a statistical
> model of neutral molecular evolution could possibly support such
> convergence. Do you?
Yes. The number 33 is not, of itself, any indication of selection. Are
we agreed on that? What's at all interesting, even to a cursory glance,
is a difference in number of transfers among genes. The obvious theory
to explain that was suggested here by Larry Moran: that the rate of some
particular mutations is higher than others. Either the gene in question
is particularly likely to be duplicated or is particularly likely to be
functional after duplication. Larry suggested a difference in the ease
with which particular protein products can find their way into the
mitochondrion.
> And if there was such an intense mutational pressure that mutated many
> duplicate copies of a functioning gene from the mitochondrial genome to
> the nuclear genome, then it would likely happen multiple times in the
> same lineage.
Note that these gene duplications happen frequently, much more
frequently than is required to explain any arbitrarily large number of
transfers. Duplication isn't the problem. Transfer of function is the
problem.
> And at least in the case of plants, the rate mutation is
> faster in the nuclear genome compared the mitochondrial genome, so if
> everything in the gene transfer was neutral, then the greater amount of
> mutations in the nuclear genome would more quickly silence the nuclear
> copy, causing loss to the nuclear copy instead of the m copy .
That made no sense. I think the problem is that "everything in the gene
transfer was neutral" is such an ambiguous statement. The rates of
mutation are irrelevant until such time as you can compare the absolute
rate of duplication with the rate of gene transfer. You have no idea how
many duplications were necessary to produce one gene transfer.
> Likewise, there would have to be numerous neutral duplications into the
> nuclear genome before drift would cause the loss of the mitochondrial
> copy. And from what I have read, there are few examples of multiple
> duplications of functioning genes from the mitochondrial genome to the
> nuclear genome within the same lineage.
You are wrong. Mitochondrial pseudogenes are plentiful, and duplications
are frequent.
> And I doubt that there are
> enough such examples to defend a statistical model of neutral molecular
> for duplications that occurred in over 30 lineages. Do you see such
> evidence for a neutral model?
No, but I haven't looked either. This is not getting you any closer to
answering the question, though.
> Concerning the advantage of what you call "genotype A" over
> "genotype B," I saw a correlation for a proposed ranking of the
> importance of the genes to the amount of times that it duplicated. This
> may explain the advantage of genotype A over genotype B, but I now see
> that it offers no explanation for the eventual loss of the m copy in
> over 30 lineages. I clearly need to add something to my hypothesis.
Quite so, because so far your hypothesis says nothing at all.
> I
> have more ideas on it after reading the article by Adams, K.L. and
> Palmer, J.D. (2003) titles "Evolution of mitochondrial gene content:
> gene loss and transfer to the nucleus," _Molecular_ _Phylogenetics_
> _and_ _Evolution_ 29, 380-395. The article briefly reviews discusses
> the potential buildup of deleterious mutations in the mitochondrial
> genome. Now, such a buildup of deleterious mutations would not cause an
> advantage for genotype A over genotype B, but such a buildup of
> deleterious mutations would set up the nuclear copy for a rapid burst
> of adaptive substitutions.
What? That again made no sense. First, we're talking about plants, in
which the mt evolution rate is slower than the nuclear rate. Second, how
does a buildup of deleterious mutations (in which copy?) set up a burst
of adaptive substitutions?
> With all of this in mind, here is a possible scenario of gene transfers
> that occurred in over 30 lineages. This scenario requires 3 major
> steps: 1) the fixation of the duplication in the nuclear genome, 2) the
> adaptive evolution of the nuclear copy, 3) the loss of the m copy to
> drift. At first there was an advantage for more copies of the gene,
> though that meant just two more copies in the nuclear genome, so this
> led to the fixation of the duplication in nuclear genome.
Not credible. Increasing the number of copies by two is just not a
significant increase.
> Then there
> was a rapid burst of adaptive substitutions in the nuclear copy that
> reversed a buildup of moderately deleterious substitutions that fixed
> during the mitochondrial stage of the gene's ancestry.
Muller's ratchet? Why would a nuclear copy release the ratchet?
> And this burst
> of adaptation made the nuclear copy superior to the m copy so that
> there was no more selective pressure to preserve the m copy. And the m
> copy was eventually lost by drift to a silencing mutation.
At least this phase is credible, sort of.
rev.goetz
I will focus on two points: 1) comparing rates of functioning
duplications versus rates of non-functioning duplications, 2) the
possibility of nuclear genome evolution reversing moderately
deleterious substitutions (subs) that built up in mitochondrial
ancestry.
You mention that there is little junk DNA in mt genomes (the original
topic) so we will not see gene-size chunks of non-functioning
duplicated from the mt genome into the nuclear genome. This is a
misconception because mutational processes that generate duplications
have no conscience related to making sure that a complete gene is
duplicated. So for hypothetically example, 50 sample lineages have 4
functional genes that duplicated from the mt genome into the nuclear
genome in at least 30 lineages while no similar size chunk of
non-functioning DNA duplicated from the mt genome into the nuclear
genome in more than 5 lineages. I clarify that I do not have the data
to support this, but such a difference of rates of functioning
duplications versus rates of non-functioning duplications would support
that natural selection was driving the fixation of the duplications
instead of random drift. Do you agree or disagree?
I am sure that if I had enough time, I could compile the data required
for such a test. And the results would either confirm or refute my
hypothesis. Unfortunately, I do not have enough time to compile this
data in the near future. (Or perhaps a researcher already as this data
compiled; do you know anybody that we could email about this?) Despite
my time constraints, it is possible to test if the functional gene
duplications from the mt genome into the nuclear genome are consistent
with either natural selection of random drift. On the other hand, if
the statistical testing suggests natural selection, this will not tell
us why there was natural selection driving the functioning gene
duplications. And you reject that an additive effect would select two
nuclear copies because there are several more mt copies. And I do not
know how we could test this.
Now I will address point 2. Other literature suggests that moderately
deleterious mutations may build up in mt genes. And in my last post I
proposed that selection in the nuclear copy could reverse moderately
deleterious subs that built up in the mt copy. For example, if there
was a deleterious sub with a 3% disadvantage in the mt gene (for
instance an A to G sub), upon duplication into the nuclear genome the
nuclear copy would need to generate only 100 G to A mutations before
there would be a nearly 1 probability that G would fix in the nuclear
locus and reverse the 3% disadvantage that originated in the mt genome.
And in most gene loci with G in nuclear genomes in a large population,
it does not take much evolutionary time to generate 100 G to A
mutations. And if there were a few such deleterious loci in the mt
genes, then the nuclear copy would quickly become superior and the mt
copy may become negligible. Unfortunately, it is hard to test for a
burst of adaptive subs when the adaptations occurred over 80 million
years ago due to saturation by drift in the following years.
John Harshman
True, but most numts seem to be rather longer than any single
mitochondrial gene, so the odds of a complete copy of at least one gene
are quite high.
(Are you familiar with the term "numt"? It means nuclear mitochondrial
sequence, i.e. a nuclear copy of a mitochondrial sequence.)
> So for hypothetically example, 50 sample lineages have 4
> functional genes that duplicated from the mt genome into the nuclear
> genome in at least 30 lineages while no similar size chunk of
> non-functioning DNA duplicated from the mt genome into the nuclear
> genome in more than 5 lineages. I clarify that I do not have the data
> to support this, but such a difference of rates of functioning
> duplications versus rates of non-functioning duplications would support
> that natural selection was driving the fixation of the duplications
> instead of random drift. Do you agree or disagree?
Disagree. What you need is some idea of the frequency of numt events of
different lengths. I contend (from what numts I have seen) that they
generally are longer than the average gene, so would tend to contain at
least one complete gene. If fragments containing full genes tend to be
fixed at a higher frequency than suggested by their occurrence as
mutations, then you have something.
> I am sure that if I had enough time, I could compile the data required
> for such a test. And the results would either confirm or refute my
> hypothesis. Unfortunately, I do not have enough time to compile this
> data in the near future. (Or perhaps a researcher already as this data
> compiled; do you know anybody that we could email about this?) Despite
> my time constraints, it is possible to test if the functional gene
> duplications from the mt genome into the nuclear genome are consistent
> with either natural selection of random drift. On the other hand, if
> the statistical testing suggests natural selection, this will not tell
> us why there was natural selection driving the functioning gene
> duplications. And you reject that an additive effect would select two
> nuclear copies because there are several more mt copies. And I do not
> know how we could test this.
It's not a matter of testing, just logic. If there are dozens or
hundreds of mitochondria in a cell, will one or two nuclear copies make
a significant difference in expression? How could they?
> Now I will address point 2. Other literature suggests that moderately
> deleterious mutations may build up in mt genes.
Not just mt genes. Nuclear genes too. Recombination of course can help
dispose of these in nuclear genes but not (we think) in mt genes.
> And in my last post I
> proposed that selection in the nuclear copy could reverse moderately
> deleterious subs that built up in the mt copy. For example, if there
> was a deleterious sub with a 3% disadvantage in the mt gene (for
> instance an A to G sub), upon duplication into the nuclear genome the
> nuclear copy would need to generate only 100 G to A mutations before
> there would be a nearly 1 probability that G would fix in the nuclear
> locus and reverse the 3% disadvantage that originated in the mt genome.
> And in most gene loci with G in nuclear genomes in a large population,
> it does not take much evolutionary time to generate 100 G to A
> mutations.
Does it take a longer or shorter time to generate those mutations in a
mt gene than a nuclear gene? Consider copy number, turnaround time, and
mutation rate in your answer.
> And if there were a few such deleterious loci in the mt
> genes, then the nuclear copy would quickly become superior and the mt
> copy may become negligible. Unfortunately, it is hard to test for a
> burst of adaptive subs when the adaptations occurred over 80 million
> years ago due to saturation by drift in the following years.
This explanation, I will note, doesn't account for differences among
genes in propensity to be transferred to the nucleus. We would expect it
to affect all genes about the same. Wouldn't we?
ErikW
> rev.goetz wrote:
> > John Harshman wrote:
snip
> >>I'm asking you to provide any suggestion of a reason why the fixation of
> >>a nuclear copy of rps1 might conceivably have been promoted by
> >>selection. I'm not claiming that drift was responsible for that
> >>fixation. I don't know. But at least drift is credible.
> >
> >
> > First, I will say that I doubt that drift is a credible explanation for
> > 33 convergent duplications of a functioning gene, unless we see a
> > "similar pattern of convergence with a gene sized chunk of
> > nonconserved" DNA that duplicated from the mitochondrial genome to
> > the nuclear genome.
>
> There is no such DNA in the typical mitochondrion. Mitochondria tend to
> have almost no junk DNA.
A little info may be appreciated. Plant mitochondria vary a lot in size
and structure (180-2400kbp according to one source). The difference is
only in a small part due to more genes; mostly what is added in a
larger mt is non-coding DNA, much of which is repetitive. Some of it
comes from the chloroplast or nucleus but the majority of it probably
comes from duplications (AFAIK). Also it is actually rare that the mt
genome consist of a single circular molecule, mostly there are several
which can undergo recombination.
I don't think enough is known about plant mitochondria to detect a
"similar pattern of convergence with a gene sized chunk of nonconserved
DNA that duplicated from the mitochondrial genome to the nuclear
genome".
ErikW
snip
Martin Striz
do mitochondria have to replicate that often compared to the nucleus of
the same cell? That would depend on the lifetime of a mitochondrion and
its standing population in the cell. <<
Mitochondria replicate independently of the cell, but their replication
is dependent on some genomic proteins, whose expression and
availability is going to be a function of the cell's replication cycle.
So most mitochondria replicate once per cell generation, although some
replication to replace lost MTs occurs.
That being said, mitochondria produce more than enough energy for
themselves and their host cell, so there aren't any major selection
pressures acting on them. Certaily, if the host cell can deal with the
wasted resources of replicating all the excess genetic material in its
genome, mitochondria could do so as well. If you look at the size of
mitochondrial genomes throughout the living world, you'll find a large
variety (Harwell's "Genetics: From Genes to Genomes" has a nice
illustration). Some mtDNA is huge, and it doesn't seem to correlate
with the complexity of the organism at all. More than likely, it's
mostly based on genetic drift.
Never overlook non-adaptive solutions.
Martin Striz
John Harshman
> John Harshman wrote:
[snip]
>>>And if there were a few such deleterious loci in the mt
>>>genes, then the nuclear copy would quickly become superior and the mt
>>>copy may become negligible. Unfortunately, it is hard to test for a
>>>burst of adaptive subs when the adaptations occurred over 80 million
>>>years ago due to saturation by drift in the following years.
>>
>>This explanation, I will note, doesn't account for differences among
>>genes in propensity to be transferred to the nucleus. We would expect it
>>to affect all genes about the same. Wouldn't we?
>
> I assume that it would take a shorter time to generate the same
> mutations in the mt gene population.
Under what assumptions of population size and relative mutation rates?
> But many geneticists conjecture
> that there is little or no recombination in the mt genome. If this is
> true, then for the most part the entire mt genome is selected for or
> against instead of selection acting on various mt loci. So a particular
> sub at a nuclear locus may have a 3% advantage while the same sub at
> the homologous locus in the mt copy would have a much smaller percent
> of selective advantage in terms of the entire mt genome.
What model of selection is this? I don't think of one that would have
the effects you claim here. A mutation that has a 3% advantage with
recombination should have the same advantage without recombination. Of
course in the latter case the rest of the mt genome would be carried
along as a hitchhiker.
> And if the
> percent of selective advantage for the respective mt genome is small
> enough, then it would be nearly neutral in the mt genome as opposed to
> the same mutation having a 3% advantage at the nuclear locus.
Why should the size of a linkage group affect the selective value of an
allele?
rev.goetz
> rev.goetz wrote:
>
> > John Harshman wrote:
>
> [snip]
>
> >>>And if there were a few such deleterious loci in the mt
> >>>genes, then the nuclear copy would quickly become superior and the mt
> >>>copy may become negligible. Unfortunately, it is hard to test for a
> >>>burst of adaptive subs when the adaptations occurred over 80 million
> >>>years ago due to saturation by drift in the following years.
> >>
> >>This explanation, I will note, doesn't account for differences among
> >>genes in propensity to be transferred to the nucleus. We would expect it
> >>to affect all genes about the same. Wouldn't we?
> >
> > I assume that it would take a shorter time to generate the same
> > mutations in the mt gene population.
>
> Under what assumptions of population size and relative mutation rates?
Well, at first I was thinking that the putative lower mutation rate in
plant mitochondria DNA compared to plant nuclear DNA would be offset by
the greater number of mt genomes per nuclear genomes. But now I see
that I do not know the standard for evaluating mutation rates in
mitochondria. And I am not sure about all of the factors involved with
mutation rates and other population dynamics with mitochondria. For
example, even if they conjugate, it would for the most part be limited
to the population within the host so I guess that this would
drastically reduce the effective population size. And I never worked
with the mathematics of any haploid population, let alone the unique
limits with mitochondria. And I have heard a lot of different things
about mutation rates in mitochondria such as big differences between
various taxa. And I heard about big differences in animal studies,
which I have not closely examined. So I assume that it can varies by
taxa and there is more unknown about mitochondria mutations rates as
compared to nuclear mutation rates.
>
> > But many geneticists conjecture
> > that there is little or no recombination in the mt genome. If this is
> > true, then for the most part the entire mt genome is selected for or
> > against instead of selection acting on various mt loci. So a particular
> > sub at a nuclear locus may have a 3% advantage while the same sub at
> > the homologous locus in the mt copy would have a much smaller percent
> > of selective advantage in terms of the entire mt genome.
>
> What model of selection is this? I don't think of one that would have
> the effects you claim here. A mutation that has a 3% advantage with
> recombination should have the same advantage without recombination. Of
> course in the latter case the rest of the mt genome would be carried
> along as a hitchhiker.
>
> > And if the
> > percent of selective advantage for the respective mt genome is small
> > enough, then it would be nearly neutral in the mt genome as opposed to
> > the same mutation having a 3% advantage at the nuclear locus.
>
> Why should the size of a linkage group affect the selective value of an
> allele?
I have a better answer for this. Selective advantage is relative to the
respective locus. And the size of the linkage group is the size of the
locus. And for hypothetical example we will use a simple model and
suppose that all functional gene domains have equal importance. In this
case, a mutation with a 3% advantage on a locus with 2 domains would
have a .3% advantage if the homolog was on a locus with 20 domains.
John Harshman
Yes, mt mutation rates vary considerably among taxa. But I don't think
less is known about them, or about their variation, than about nuclear
mutation rates. Since we're talking about angiosperms here, you should
probably work with those rates, which as you know are very low.
>>>But many geneticists conjecture
>>>that there is little or no recombination in the mt genome. If this is
>>>true, then for the most part the entire mt genome is selected for or
>>>against instead of selection acting on various mt loci. So a particular
>>>sub at a nuclear locus may have a 3% advantage while the same sub at
>>>the homologous locus in the mt copy would have a much smaller percent
>>>of selective advantage in terms of the entire mt genome.
>>
>>What model of selection is this? I don't think of one that would have
>>the effects you claim here. A mutation that has a 3% advantage with
>>recombination should have the same advantage without recombination. Of
>>course in the latter case the rest of the mt genome would be carried
>>along as a hitchhiker.
>>
>>
>>>And if the
>>>percent of selective advantage for the respective mt genome is small
>>>enough, then it would be nearly neutral in the mt genome as opposed to
>>>the same mutation having a 3% advantage at the nuclear locus.
>>
>>Why should the size of a linkage group affect the selective value of an
>>allele?
>
> I have a better answer for this. Selective advantage is relative to the
> respective locus. And the size of the linkage group is the size of the
> locus. And for hypothetical example we will use a simple model and
> suppose that all functional gene domains have equal importance. In this
> case, a mutation with a 3% advantage on a locus with 2 domains would
> have a .3% advantage if the homolog was on a locus with 20 domains.
No, all you have done is to restate your assumption. It's not an answer.
And in fact this assumption makes no sense. Selective value does not
depend on the size of the genome or linkage group. It depends on the
mean differential reproductive success of genotypes including that
particular allele vs. other alleles at the same locus. Did you make up
this model personally? I doubt you could have read about it anywhere.
rev.goetz
Well, I was originally referring to data compiled in the review by
Lang, Gray, and Burger (1999) that includes gene transfer data in
protists, plants, fungus, and animals. So I need to see mutation rate
data that compares sample mt rps genes versus nuclear rps genes in all
of the respective taxa. And from what you say, I assume that this
information is available but I do not have readily accessible to me.
I do not recall all of the bibliography of my readings on
recombination. But in this context I want to make sure that we
understand the definition of "allele." For example, let us consider
a hypothetical case of a genome with a single chromosome that has no
recombination. If an advantageous mutation occurs on a particular gene
in the hypothetical chromosome that has no recombination, then the
entire chromosome is the mutant allele. This means that the entire
chromosome is under selection as opposed to a specific locus on the
chromosome. Do you agree or disagree?
John Harshman
If the data exist, a little work with GenBank should provide them for
you. Searching on rps-1 (or whatever) should find most of them.
Generally not called that. It's a haplotype. The distinction is fuzzy,
but there you are. However, I don't think it matters.
> This means that the entire
> chromosome is under selection as opposed to a specific locus on the
> chromosome. Do you agree or disagree?
You can think about it both ways. Either way, your idea that selection
is diluted by the size of a linkage group is not supported.
Friar Broccoli
> There are mitochondria with junk. In fact the control region
> has been duplicated several times in different groups of
> birds, and one of the copies is clearly non-functional. So it
> does happen. But why so rarely?
OK John I am going to extend my neck onto the chopping block and
propose the answer which popped into my tiny little brain soon
after I read this question so very long ago:
To me it seems reasonable that it is primarily a byproduct of mt
DNA being passed exclusively down the female line.
As I see it most useful conserved mutations occur in the main
part of the cell because when a useful mutation occurs there it
can be spread efficiently through the rest of the population by
sexual dispersal. Beneficial mutations in mt by contrast can
only become prevalent by eliminating all other female lines.
In many cases dispersing a beneficial mutation will imply
spreading any junk DNA that the founder of the benefit happened
to be carrying at the time he acquired the beneficial
adaptation. When an mt mutation becomes prevalent all the junk
accumulated by other females in separate lines is removed.
My thinking may be a bit muddled on this, but I believe this
also explains why plants have more junk in their DNA. Plant
reproduction involves many more female eggs (or whatever they
are called in plants) making speciation events more rare.
According to my foggy conception speciation events are usually
associated with genetic bottle necks which would clean out the
variations in mt, but be far less hard on the DNA in the main
body of the cell which is shared by most members of the
population most of the time.
Finally, the copying limitations of mt mention by Larry Moran
and more obviously the fact that it makes no sense for a
virus/phage to invade mitochondrial DNA as mentioned by r norman
would further decrease the amount of junk seen.
He said, crawling away into his hole in expectations of a
withering attack.
Cordially;
Friar Broccoli
Robert Keith Elias, Quebec, Canada Email: EliasRK (of) gmail * com
Best programmer's & all purpose text editor: http://www.semware.com
--------- I consider ALL arguments in support of my views ---------